ABSTRACT

Acne scarring is often challenging to manage. Various laser treatments are helpful in addressing abnormal color and texture in order to improve the appearance of an acne scar. This paper will review the appropriate use and side-effects of these laser treatments.

Key Words:
acne vulgaris, laser therapy, scarring

Introduction

Scarring caused by inflammatory acne is extremely bothersome to the patient and often challenging to treat. The senior author uses a classification method for acne scarring based on both color and texture (Table 1).¹ Both features must be addressed independently in order to improve the visible quality of the scar. Topical, physical, surgical, and light modalities may be used alone or in combination to improve the appearance of acne scars. This paper specifically addresses laser modalities to treat abnormalities in color and texture in acne scarring.

Laser Options Targeting Skin Color

Red Scars

Erythema is the result of visible dilated capillaries beneath the skin surface. The intensity of the erythema is dependent on the concentration, lumen size, and depth of blood vessels. Lasers and light sources used to decrease erythema of acne scars include the pulsed dye laser (PDL), potassium-titanyl-phosphate (KTP) laser, intense pulsed light (IPL), and neodymium:yttrium-aluminumgarnet (Nd:YAG) laser. Suggested laser settings are shown in Table 2. The number of treatments will vary according to several factors including patient response after each laser session, laser technology used, and parameters of treatment.

PDL is the gold standard for treating erythema from acne scarring.² This laser has an output wavelength of 585 nm or 595 nm, targeting oxyhemoglobin within red blood cells by approximating a major hemoglobin absorption peak at 577 nm. Treatments may be safely performed on all skin types and over hair-bearing areas without fear of follicular destruction. Tolerability of laser treatments is improved with dynamic cooling in the form of cryogen spray. Purpura occurs with extravasated red blood cells, indicating immediate vascular photocoagulation. It is advocated as a clinical endpoint of treatment, lasting a maximum of 7-10 days and resolving without sequelae.

The KTP, or frequency-doubled Nd:YAG laser, has an output wavelength of 532 nm, targeting the first peak of the oxyhemoglobin absorption curve. The penetrative depth of the KTP laser is confined to the papillary dermis of the skin and unsuitable for deeper vessels. KTP lasers generally cause only mild purpura and minimal postinflammatory hyperpigmentation on all skin types.

IPL systems are comprised of noncoherent light (approximately 500-1200 nm) released by a flashlamp within the device, which is then filtered to narrower ranges of wavelengths that simulate the monochromatic nature of true laser light. IPL devices have the benefit of larger spot sizes and a wider range of pulse duration and fluences, thereby allowing for treatment at greater depth and faster speed, coverage of larger surface areas, and concurrent therapy of multiple conditions. However, specificity for treating a single condition may be poor due to absorption competition from multiple tissue targets. Postinflammatory hyperpigmentation in darker skin types may be seen with IPL therapy.³

Nd:YAG lasers may be useful for treating erythema in scars with dilated blood vessels in the deep dermis. New microsecondpulsed Nd:YAG lasers are of benefit for targeting superficial dermal vessels due to the short pulse duration, low fluence, and quick repeated laser bursts.

Brown Scars

Hyperpigmentation of acne scars is common, particularly with darker skin types. Lasers used to treat scar hyperpigmentation include IPL, quality-switched (Q-switched), microsecond-pulsed Nd:YAG, both confluent and fractionated ablative erbium:YAG (Er:YAG), and yttrium-scandium-gallium-garnet (YSGG). Suggested laser settings are presented in Table 3. Concomitant use of lightening creams and sunscreen, as well as sun avoidance, is advocated to further reduce scar contrast with surrounding skin.

IPL devices, with their ability to vary output wavelength, pulse duration, and fluence, can treat several skin conditions including superficial pigmentation.³ Care must be taken to protect the epidermis from overheating, which may cause pigment incontinence and further hyperpigmentation. Parallel cooling (extracting heat from the epidermis during the light pulse) is usually provided through the use of a sapphire window handpiece that generates surface cooling to approximately 5°C.

Q-switched lasers have the unique property of extremely short pulse durations, thereby allowing these devices to target very small pigment cells and particles, such as melanocytes, with minimal competition from the hemoglobin absorption curve. The Q-switched lasers, i.e., ruby (694 nm), alexandrite (755 nm), and Nd:YAG (1064 nm), are useful for treating skin pigmentation.⁴ The endpoint of treatment is mild superficial crusting. Care must be taken to use the lowest energy settings possible to achieve pigment reduction, as too much energy may result in punctate bleeding, cell rupture, scarring, and increased pigmentation.

Microsecond-pulsed Nd:YAG lasers (1064 nm) target both melanin pigment and small blood vessels to reduce erythema and stimulate collagen production without inducing injury to surrounding tissue. This laser may be used for any skin type.⁵

Confluent laser treatment involves laser light striking the entire surface of the skin in a given area, whereas fractionated laser therapy creates microscopic thermal wounds while sparing adjacent tissue over the targeted site.⁶ Confluent ablative Er:YAG (2940 nm) and YSGG (2790 nm) lasers have tremendous water absorption capacity, translating into vaporization of surface tissue with minimal collateral heating, limited damage to surrounding tissue, and reduced risk for further hyperpigmentation.⁷ These lasers ablate approximately 30 microns of the epidermis, inducing exfoliation and improving superficial hyperpigmentation. Test spots should be performed when using any ablative laser on darker skin.

Fractionated ablative Er:YAG and YSGG lasers release light energy at high peak power to create channels in skin tissue.⁶ These channels are physically ablated, leaving true air channels that allow removal of surrounding pigment via transepidermal elimination.

White Scars

Ultraviolet (UV) light stimulates melanogenesis in areas where melanocytes are intact. UV light can stimulate the migration of melanin-producing cells to melanocyte-deficient areas, increasing pigment in these regions.¹ Excimer (excited dimer) lasers have a wavelength in the UV range (308 nm), providing concentrated melanin stimulation to white scars.

Fractionated ablative lasers (Er:YAG, YSGG, and carbon dioxide) create air channels that ultimately contract to reduce the surface area of the white scars, making them appear smaller in diameter.⁷

Laser Options Targeting Skin Texture

Hypertrophic Scars

When evaluating a scar that exhibits both color and elevation defects, it is preferrable to treat the texture before addressing the color, because both vascular-targeting and pigment-targeting lasers provide optimal penetration through scars that are flat and soft.¹ Topical corticosteroids, alone or in combination with intralesional corticosteroids, used concomitantly with laser therapy are recommended to achieve softening and flattening of elevated scars.

Fractionated ablative lasers (Er:YAG, YSGG, and carbon dioxide) can help soften elevated scars by ablating channels of condensed collagen that contribute to the scar’s thickness and firmness.⁷ Fractionated ablative and nonablative lasers must be used with caution in softening elevated scars because their collateral thermal damage has the profibrotic potential to further thicken and harden scar tissue. As an aside, fractionated ablative laser treatment may also improve topical drug delivery by providing a theoretical route for transepidermal drug penetration via ablative channels created by the laser.⁸

Confluent ablative laser treatment (Er:YAG, YSGG, and carbon dioxide) has been shown to decrease the size and thickness of scar recurrence after surgical excision, provided laser therapy is performed at the base of the excised area immediately after surgical removal.⁹ Repeated pulses to the base of the excised tissue establish hemostasis and thin eschar formation. A viscous moisturizer (e.g., petrolatum) under occlusion should be applied for 3 days post-treatment, followed by a nonviscous moisturizer until the skin re-epithelializes. At the first sign of recurrent scar formation, topical corticosteroids or imiquimod are suggested to prevent progression of fibrosis.

Atrophic Scars

Depressed (Icepick and Boxcar) Scars

In treating icepick and boxcar scars, the goals are to soften the edges between the indentation and surrounding normal skin, and stimulate collagen production within the depressed area.

Resurfacing of depressed facial scars with confluent ablative Er:YAG, YSGG, and carbon dioxide lasers causes thermal injury to the epidermis and a portion of the dermis, resulting in vaporization, collagen injury, and re-epithelialization. In particular, Er:YAG lasers are highly selective for water, therefore leading to maximal tissue vaporization and reduced residual thermal damage. These devices decrease post-treatment erythema, are safe for use on darker skin types, and preferred for superficial atrophic scars due to shorter recovery times. The production of increased dermal fibrotic elements through greater collateral thermal heating capacity is enhanced with use of the YSGG and carbon dioxide lasers, making them more beneficial for deeper scars. Ablation typically requires 1 pass with the carbon dioxide laser at 300 mJ, 1-2 passes with the YSGG laser at 3.5 J/cm², and 2-3 passes with the Er:YAG laser at 5 J/cm². Deep treatment with the Er:YAG laser typically results in bleeding due to its limited effects on blood vessel photocoagulation.

Confluent nonablative laser treatment such as PDL, IPL, microsecond-pulsed, and Q-switched Nd:YAG lasers, as well as a variety of lasers operating in the near infrared spectrum (e.g., 1320 nm, 1440 nm, 1450 nm, 1540 nm, and 1550 nm) target water within the deeper aspects of the dermis more efficiently, thereby creating bulk heating and more collagen stimulation, referred to as subsurfacing.¹⁰ Subsurfacing may be painful, often requiring systemic analgesia.

Fractionated ablative laser treatment creates microscopic channels of thermal injury on the skin, causing skin tightening and smoothening through ablation and re-epithelialization, as well as elevation of the floor of depressed scars through collagen remodelling.¹¹ Ablative fractional resurfacing is gentler on the skin compared with confluent resurfacing and can be safer for darker skin types; however, test spots should be performed before attempting laser resurfacing on this subset of patients. Er:YAG laser treatment is preferred for small diameter icepick and boxcar scars and for larger diameter defects in darker skin types; fractionated YSGG and fractionated carbon dioxide lasers are favored for icepick and boxcar scarring in white-skinned individuals.¹

Nonablative fractional resurfacing lasers produce wavelengths in the mid-infrared range and include fractionated 1440 nm, 1450 nm, 1540 nm, and 1550 nm lasers. Nonablative lasers create zones of microthermal skin injury, requiring minimal downtime. However, the treatment process may be painful to the point of requiring oral analgesia.

Depressed (Rolled) Scars
With rolled acne scarring, treatment success depends on the degree to which the skin is bound down at the base of the scar. If the skin contour is tightly tethered, it is advisable to perform surgical subcision before other treatments to loosen the surface adhesion and dampen the tethering effect.¹² Care should be taken to wait at least 2 weeks post-filler placement before attempting fractionated ablative or nonablative laser resurfacing to avoid disruption of filler placement.

Both confluent and fractionated nonablative laser treatments and fractionated ablative laser therapy may be used for rolled scars. In all cases, it is important for the laser energy to reach deeper components of the skin in order to stimulate collagen remodelling and weaken tethering adhesions.

Conclusion

Lasers are an important treatment option in the management of acne scarring as they can target both color and textural abnormalities. It is essential to understand both the pathophysiology of these skin defects as well as the distinct mechanisms and clinical effects of each laser. Such an appreciation enables selection of the most appropriate device and technique in order to optimize outcomes for a given patient.

References

1. Rao J. Treatment of acne scarring. Facial Plast Surg Clin North Am 2011 May; 19(2):275-91.
2. Alster TS, McMeekin TO. Improvement of facial acne scars by the 585 nm flashlamp-pumped pulsed dye laser. J Am Acad Dermatol 1996 Jul;35(1):79-81.
3. Ho SG, Chan HH. The Asian dermatologic patient: review of common pigmentary disorders and cutaneous diseases. Am J Clin Dermatol 2009; 10(3):153-68.
4. Kim S, Cho KH. Treatment of facial postinflammatory hyperpigmentation with facial acne in Asian patients using a Q-switched neodymium-doped yttrium aluminum garnet laser. Dermatol Surg 2010 Sep;36(9):1374-80.
5. Min SU, Choi YS, Lee DH, et al. Comparison of a long-pulse Nd:YAG laser and a combined 585/1,064-nm laser for the treatment of acne scars: a randomized split-face clinical study. Dermatol Surg 2009 Nov;35(11):1720-7.
6. Tierney EP, Hanke CW. Review of the literature: Treatment of dyspigmentation with fractionated resurfacing. Dermatol Surg 2010 Oct;36(10):1499-508.
7. Ross EV, Swann M, Soon S, et al. Full-face treatments with the 2790-nm erbium:YSGG laser system. J Drugs Dermatol 2009 Mar;8(3):248-52.
8. Haedersdal M, Sakamoto FH, Farinelli WA, et al. Fractional CO(2) laserassisted drug delivery. Lasers Surg Med 2010 Feb;42(2):113-22.
9. Morosolli AR, De Oliveira Moura Cardoso G, Murilo-Santos L, et al. Surgical treatment of earlobe keloid with CO2 laser radiation: case report and clinical standpoints. J Cosmet Laser Ther 2008 Dec;10(4):226-30.
10. Bhatia AC, Dover JS, Arndt KA, et al. Patient satisfaction and reported longterm therapeutic efficacy associated with 1,320 nm Nd:YAG laser treatment of acne scarring and photoaging. Dermatol Surg 2006 Mar;32(3):346-52.
11. Hedelund L, Moreau KE, Beyer DM, et al. Fractional nonablative 1,540-nm laser resurfacing of atrophic acne scars. A randomized controlled trial with blinded response evaluation. Lasers Med Sci 2010 Sep;25(5):749-54.
12. Alam M, Omura N, Kaminer MS. Subcision for acne scarring: technique and outcomes in 40 patients. Dermatol Surg 2005 Mar;31(3):310-7.

Division of Dermatology and Cutaneous Sciences, University of Alberta, Edmonton, AB

Introduction

Scarring, whether from planned surgical procedures or a sequela of inflammatory conditions such as acne, striae, burns or trauma, is often associated with considerable emotional impact. As a result, patients often seek the advice of physicians regarding scar revision. This paper focuses on a comprehensive and practical approach to classifying and managing scars in terms of colour and texture, and discusses topical treatments accessible to family physicians in more detail.

Scar Formation

• Scars are part of the normal healing process after cutaneous injury. The process is part of the remodeling phase of wound repair, following the phases of hemostasis and inflammation.
  • The wound repair phase involves re-epithelialization, neocollagenesis, neovascularization, and pigment deposition.
• Scar formation can take up to months to fully realize the severity and extent. Once the skin re-epithelializes (i.e., wound closure is established and intact), the structural integrity of the injured site should be amenable to most scar treatment protocols, which may then be initiated.
• Patients undergoing scar treatment should be cautioned to avoid direct sun exposure whenever possible to prevent excess vascular or pigment deposition in the repaired tissue.

Classification of Scars

• All scars can be categorized according to both colour and texture (Tables 1 and 2). Both of these components must be considered and addressed independently to attain improvement of the visible quality of the scar.¹
• Active inflammation must first be resolved before determining the correct classification of a scar. Inflammation is characterized by a purple discoloration, tenderness, and focal elevation of the skin.

Treatment Options

• Every scar can be broken down and categorized according to colour and texture, both of which must be addressed independently to improve the scar’s appearance.
• This paper will focus mainly on topical therapies used to improve the appearance of scars, although tables with comprehensive options for scar revision are presented.

Treatment Options Targeting Scar Colour

Table 3 lists comprehensive options targeting scars with abnormal colour. Topical therapies within each category will be discussed in more detail.

• Cosmetic camouflage using makeup creams and powders in a patient’s normal skin tone will help conceal the abnormal scar colour.
• Topical vasoconstrictors such as oxymetazoline, epinephrine or cocaine may be used to constrict blood vessels, decreasing a scar’s redness.
• Lightening creams containing hydroquinone, azelaic acid or kojic acid may be helpful to decrease brown hyperpigmentation.
• Hydroquinone 2%-5% alters conversion of dopa to melanin by inhibiting the activity of tyrosinase. Side-effects include allergic and irritant contact dermatitis, post-inflammatory hyperpigmentation, and cutaneous ochronosis. Animal studies have shown teratogenicity and induction of renal adenoma, but these findings have not been seen in humans.⁴
• Kojic acid 2% is a tyrosinase inhibitor produced by fungi such as Aspergillus oryzae. Side-effects may include irritation.
• Azelaic acid 15% (Finacea®) is a tyrosinase inhibitor and may be antiproliferative and cytotoxic towards melanocytes. Side-effects include erythema, scale, burning, and pruritus.
• Topical retinoids such as tretinoin 0.01%-0.1% (Retin-A Micro®, Stieva-A®), adapalene 0.1%-0.3% (Differin®, Differin® XP™), and tazarotene 0.1% (Tazorac®) may reduce brown pigmentation by inhibiting tyrosinase transcription, interrupting synthesis of melanin. Side-effects include xerosis, erythema, skin peeling, and sun sensitivity.
• Chemical peels involve the application of a chemical agent on the skin, causing controlled destruction of parts of the epidermis and dermis, potentially decreasing hyperpigmentation. This leads to exfoliation and later epidermal and dermal regeneration. Common chemical peel agents include alpha hydroxy acids (glycolic acid, lactic acid), beta hydroxy acids (salicylic acid) and trichloroacetic acid. Depth of the chemical peel varies depending on the chemical agent chosen. This should be done in consultation with a dermatologist. Side-effects may include pigmentary changes, infection, erythema, and scarring.⁵
• Topical calcineurin inhibitors such as tacrolimus 0.03%- 0.1% (Protopic™) and pimecrolimus 1% (Elidel®) have immunomodulatory effects that may help with repigmentation of white scars. Side-effects include burning and pruritus. Although the US FDA has a black box warning on these therapies regarding risk of lymphoma and skin cancer development, clinical evidence in humans has not suggested causality.⁶
• Silicone gels have been shown to reduce the redness of scars.⁷

Treatment Options Targeting Scar Texture

Table 4 lists comprehensive options targeting scars with abnormal texture. Topical therapies within each category will be discussed in more detail.

• Elevated scars
  • Strategies for prevention of hypertrophic and keloid scars during surgical procedures include minimizing tension and everting wound edges during closure, avoiding anatomic locations more prone to hypertrophic or keloid scars such as across joints, angle of the jaw, shoulders, mid-chest, and upper back, placing incisions in areas that follow skin creases, and achieving efficient hemostasis.²
  • Very high potency topical corticosteroids such as clobetasol propionate 0.05% (Dermovate®) or halobetasol propionate 0.05% (Ultravate®) ointments or creams may be used for minimally hypertrophic scars. They are usually ineffective with more hypertrophic or keloid scars.
  • Intralesional corticosteroids such as triamcinolone 10-40 mg/mL (Kenalog®) may help decrease the elevation seen in hypertrophic and keloid scars.
  • Corticosteroids act to suppress the immune responses as well as diminish collagen synthesis, inhibit fibroblast growth, and enhance collagen degeneration. Adverse effects of topical and intralesional corticosteroids include hypopigmentation around the injection site, dermal atrophy, telangiectasia, widening of the scar, and delayed wound healing.
  • Topical imiquimod (Aldara™) is an immunomodulator that stimulates interferon-α, inducing collagen breakdown. In off-label use, studies have shown that nightly application of imiquimod to keloidal scars improves cosmetic appearance over an 8-week period. Adverse effects of imiquimod include erythema and irritation.^8,9
  • Over-the-counter (OTC) topical silicone gel products (e.g., Kelo-cote® and Dermatix™ Ultra) applied twicedaily for 4 months have also shown beneficial effects on both treatment and prevention of hypertrophic and keloid scars.
    • The postulated mechanism of action involves reducing transepidermal water loss (TEWL), enhancing hydration, and decreasing activation of dermal fibroblasts through inhibition of cytokine production. These combined processes normalize collagen deposition and diminish scar hypertrophy.¹⁰
    • Silicone gel may be used for existing and new hypertrophic and keloid scars resulting from burns, surgical procedures, trauma, and wounds. Treatment has been shown to reduce redness, hardness, elevation, itching, and pain.^7,10
    • For post-surgical or -trauma treatment, it may be considered a first-line prophylactic strategy in the prevention and development of hypertrophic or keloidal scars.¹¹
    • Both gel and sheet products have comparable efficacy, but for greater practical contouring of flexural areas gels may be preferred, as optimal occlusion is achieved by close apposition of the product with the scar.¹⁰
    • The gel is well-tolerated with no common adverse effects.⁹
    • Spray formulations are especially useful on sensitive or larger skin areas.
    • Preparations containing silicon dioxide dry rapidly, allowing for cosmetics or sunscreen application over the silicone treatment.
  • Occlusive dressings such as pressure dressings and silicone gel sheeting (Cica-Care™) are commonly used to treat burn scars. The mechanism of action is through mechanical compression and reduction in oxygen tension, along with silicone’s effects discussed above. Pressure dressings must maintain a pressure of 25-40 mmHg, up to 24 hours a day, for 9-10 months for best results. Silicone gel sheets must be used 24 hours a day for 3-4 months.^8,9
  • Topical onion extract (Mederma®) and vitamin E are widely used OTC products for scar revision, but clinical effects were not found to be significant over placebo.⁹
• Depressed scars
  • Cosmetic camouflage using makeup creams and powders in a patient’s normal skin tone will help fill in and conceal dark shadows created by the scar’s depressions.
  • Chemical peels (see treatments for scar colour) serve to exfoliate and resurface the skin’s surface, decreasing the relative depth of depressed scars.

Conclusion

• All scars can be classified by their colour and texture. A multimodal approach targeting both aspects is essential to optimal scar management.
• Many topical therapies are available to family physicians to improve scar appearance. Failing this, referral to a dermatologist for further topical, physical, light, laser, or surgical interventions for scar revision should be considered.

References

1. Rao J. Facial Plast Surg Clin North Am 19(2):275-91 (2011 May).
2. Wolfram D, et al. Dermatol Surg 35(2):171-81 (2009 Feb).
3. Jacob CI, et al. J Am Acad Dermatol 45(1):109-17 (2001 Jul).
4. Nordlund JJ, et al. J Eur Acad Dermatol Venereol 20(7):781-7 (2006 Aug).
5. Khunger N. Indian J Dermatol Venereol Leprol 74 Suppl:S5-12 (2008 Jan).
6. Patel TS, et al. Am J Clin Dermatol 8(4):189-94 (2007).
7. Sepehrmanesh M. Komp Dermatologie 1:30-2 (2006).
8. Juckett G, et al. Am Fam Physician 80(3):253-60 (2009 Aug 1).
9. Reish RG, et al. J Am Coll Surg 206(4):719-30 (2008 Apr).
10. Mustoe TA. Aesthetic Plast Surg 32(1):82-92 (2008 Jan).
11. Mustoe TA, et al. Plast Reconstr Surg 110(2):560-71 (2002 Aug).